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PA25.4 | Pulmonary Tuberculosis — SDL Guide (Part 3)

Complications of Pulmonary Tuberculosis

Multi-panel medical diagram showing local pulmonary and systemic complications arising from cavitary pulmonary tuberculosis. — **Panel A:** Central upper-lobe tuberculous cavity, caseous necrosis, cavity wall bacilli, sputum shedding, airway spread, pleural rupture route, vascular erosion route, healed fibrosis route. **Panel B:** Thick-walled cavity, enlarging cavitation, bacilli in cavity wall, bacilli shed into sputum, high infectivity. **Panel C:** Branch pulmonary artery, cavity wall erosion, Rasmussen aneurysm, rupture site, massive haemoptysis, bronchial blood. **Panel D:** Healed fibrotic scar, traction on bronchi, permanently dilated bronchi, mucus retention, recurrent secondary infection. **Panel E:** Cavity draining into bronchus, aspirated bacilli, dependent lung zones, diffuse alveolar filling, tuberculous bronchopneumonia. **Panel F:** Subpleural granuloma or cavity, pleural space, lymphocytic exudative effusion, empyema, fibrous pleural peel, trapped lung/fibrothorax. **Panel G:** Peripheral cavity rupture, air in pleural cavity, collapsed lung, visceral pleura, parietal pleura, pneumothorax. **Panel H:** Chronic inflammation, serum amyloid A, AA amyloid deposits, kidney, liver, spleen, nephrotic syndrome, hepatosplenomegaly. **Panel I:** Post-tuberculous pulmonary fibrosis, vascular obliteration, pulmonary hypertension, right ventricular hypertrophy, cor pulmonale, infected sputum, laryngeal TB, hoarseness.

Understanding complications is examining priority and clinical reality:

Local / pulmonary complications:

Cavitation — ongoing cavity enlargement with failure to heal; bacilli multiply in cavity wall and are shed into sputum (high infectivity).
Haemoptysis — erosion of a branch pulmonary artery in a cavity wall → Rasmussen aneurysm (fusiform dilatation from inflammatory weakening) → rupture → massive haemoptysis (emergency). Minor haemoptysis from granulation tissue.
Bronchiectasis — fibrous contraction and traction on bronchi after healing → permanent bronchial dilatation → recurrent secondary infections.
Tuberculous bronchopneumonia — bacilli drain from cavity into bronchi → diffuse alveolar filling in dependent zones; fulminant, high mortality.
Pleural effusion / empyema — rupture of a subpleural granuloma or cavity into pleural space → tuberculous pleuritis (exudative lymphocytic effusion) → if untreated, empyema → fibrothorax (trapped lung).
Pneumothorax — rupture of a peripheral cavity into pleural space.

Systemic / remote complications:

Secondary amyloidosis (AA type) — chronic TB produces sustained high serum amyloid A protein → amyloid deposits in kidney, liver, spleen → nephrotic syndrome, hepatosplenomegaly.
Cor pulmonale — extensive pulmonary fibrosis and vascular obliteration after healed TB → pulmonary hypertension → right ventricular hypertrophy and eventual failure.
Laryngeal TB — seeding from infected sputum → hoarseness, dysphonia; highly infectious.
Intestinal TB — swallowed sputum → ileocaecal involvement → malabsorption, stricture, fistula.
Renal / adrenal / bone TB (as above — haematogenous).

Memory anchor: "Every TB cavity can bleed (Rasmussen), collapse (pneumothorax), fill with fluid (empyema), or spread (bronchopneumonia). Untreated chronic disease causes amyloid and cor pulmonale."

CLINICAL PEARL

Rasmussen aneurysm — the most dramatic TB complication: When a pulmonary artery branch lies in the wall of a TB cavity, chronic inflammation weakens its muscular wall → pseudoaneurysm formation (Rasmussen aneurysm). Rupture causes sudden, massive haemoptysis — bright red blood in large volumes, often fatal. On HRCT, it appears as an enhancing nodule within a cavity wall. Endovascular bronchial artery embolisation is the emergency treatment. This is examined regularly because it links TB morphology directly to a life-threatening clinical emergency.

Latent TB, Reactivation Triggers, and Drug Resistance

Infographic showing latent tuberculosis within a granuloma, triggers for reactivation, and the progression from MDR-TB to XDR-TB and TDR-TB. — **Panel A:** Latent TB granuloma showing dormant M. tuberculosis bacilli, infected macrophages, Langhans giant cells, lymphocyte ring, fibrous capsule, and clinical features of LTBI.. **Panel B:** Reactivation with granuloma breakdown, bacilli escaping into airways, inflammatory lung tissue, and loss of immune containment.. **Panel C:** Major reactivation triggers: HIV/AIDS with CD4 depletion, malnutrition, diabetes mellitus, TNF-alpha inhibitors, high-dose corticosteroids, advanced age, silicosis, and haematological malignancy.. **Panel D:** Drug-resistant TB ladder showing MDR-TB, XDR-TB, and TDR-TB with crossed-out drug classes.. **Panel E:** Resistance-driving factors showing poor adherence, monotherapy, and sub-therapeutic dosing leading to drug resistance and public health threat..

Latent TB infection (LTBI): ~1.8 billion people worldwide harbour viable but dormant M. tuberculosis within granulomas. In LTBI: no symptoms, no infectious sputum, positive Mantoux/IGRA (evidence of prior sensitisation), normal chest X-ray (or only calcified Ghon lesion). Bacilli persist within macrophages in a metabolically slowed state.

Reactivation triggers (break the granuloma's immune containment):
• HIV/AIDS (most powerful — CD4 depletion destroys the immunological scaffold of the granuloma)
• Malnutrition / diabetes mellitus
• TNF-α inhibitors (used in RA, IBD) — block macrophage activation
• High-dose corticosteroids
• Advanced age
• Silicosis (silicotuberculosis)
• Haematological malignancies

Drug-resistant TB:
• MDR-TB (multidrug-resistant): resistant to at least isoniazid + rifampicin (the two most potent first-line drugs).
• XDR-TB (extensively drug-resistant): MDR-TB + resistance to any fluoroquinolone + at least one injectable second-line drug.
• TDR-TB (totally drug-resistant): resistant to all tested drugs — a clinical and public health catastrophe.
• India has among the highest MDR-TB burdens globally. Inadequate treatment (poor adherence, monotherapy, sub-therapeutic dosing) drives resistance.

Diagnosis summary:

Test	Detects	Notes
Sputum AFB smear (ZN)	Bacilli in sputum	Fast, cheap; low sensitivity (~50–60%)
Sputum culture (LJ/MGIT)	Viable bacilli + DST	Gold standard; 2–8 weeks
GeneXpert MTB/RIF (CBNAAT)	MTB DNA + rifampicin resistance	2 hours; sensitivity ~85–90%; RNTCP/NTEP first-line
Mantoux (TST)	Prior sensitisation (CMI)	Positive in latent + active; false-negative in immunosuppressed
IGRA (QuantiFERON)	IFN-γ release (CMI)	Preferred in BCG-vaccinated populations
HRCT chest	Structural disease	Cavities, miliary, adenopathy, bronchiectasis

Cavitary TB — Gross Pathology Summary

Diagram of cavitary tuberculosis showing early, established, and advanced gross lung pathology with caseous necrosis, fibrous cavity wall, satellite granulomas, fibrosis, pleural thickening, blood clot, and traction bronchiectasis. — **Panel A:** Upper lobe cavitary lesion, thick fibrous wall, caseous inner lining, satellite granulomas, surrounding fibrosis, pleural thickening, distorted bronchi, traction bronchiectasis. **Panel B:** Early cavity, grey-yellow caseous material, zone of confluence, absent defined wall, surrounding granulomas, lung parenchyma. **Panel C:** Established cavity, well-defined cavity, thick fibrous wall, dried caseous lining, chalk-white caseous material, dense fibrous bands, healed scarring. **Panel D:** Multiple cavities, blood clot from vessel erosion, compressed fibrotic lung, thickened pleura, distorted bronchi, traction bronchiectasis.

The cavitary TB lung is a stark illustration of disease progression:

Early cavity: grey-yellow caseous material filling a zone of confluence; no defined wall; surrounding granulomas visible as grey nodules in the parenchyma.
Established cavity: well-defined cavity with a thick fibrous wall; inner surface lined with dried caseous material (may appear chalk-white or grey); surrounding lung shows dense fibrous bands (old scarring from healed prior disease).
Advanced disease: multiple cavities, varying size; some contain blood clot (from vessel erosion); surrounding lung compressed and fibrotic; pleura thickened; bronchi distorted (traction bronchiectasis).

A labeled medical illustration shows an upper-lobe secondary tuberculosis cavity with caseous lining, fibrous wall, satellite granulomas, surrounding fibrosis, pleural thickening, and a clinical MDR-TB classification inset. — **Panel A:** Longitudinal lung section; upper lobe cavity; thick fibrous wall; caseous inner lining; satellite granulomas; surrounding fibrosis; pleural thickening; bronchus; lower lobe parenchyma.. **Panel B:** Magnified cavity wall showing pleural thickening, fibrous wall, granulomatous inflammation, Langhans-type giant cell region, and central caseous necrosis.. **Panel C:** Clinical flow showing smear-positive TB after 4 months, GeneXpert rifampicin resistance, presumptive MDR-TB, DST panel, and referral to DR-TB centre under NTEP..

SELF-CHECK

A 45-year-old male with smear-positive TB on RNTCP treatment for 4 months is found to have persistent AFB on sputum smear. GeneXpert detects rifampicin resistance. What is the correct classification?

A. XDR-TB — because he has failed all first-line drugs

B. Latent TB — because smear positivity after 4 months indicates dormant bacilli

C. MDR-TB — resistance to at least isoniazid and rifampicin confirmed

D. Drug-susceptible TB — rifampicin resistance alone is not sufficient for MDR classification

Reveal Answer

Answer: C. MDR-TB — resistance to at least isoniazid and rifampicin confirmed

MDR-TB is defined as resistance to at least isoniazid AND rifampicin. GeneXpert detects rifampicin resistance as a proxy for MDR-TB (because rifampicin resistance almost never occurs in isolation without concurrent isoniazid resistance in clinical practice). XDR-TB additionally requires resistance to fluoroquinolones and injectable second-line drugs. This patient needs a Drug Susceptibility Test panel and referral to a DR-TB centre under NTEP.